Cardiovascular Physiology Past Paper PDF

**[Chapter 14 -- Cardiovascular Physiology \~ Start of Exam 3]** 1. [Describe the membrane proteins and ion movement involved in myocardial excitation-contraction (EC) coupling and relaxation]. **CONTRACTION**: AP starts in pacemaker cell & AP enters from adjacent cell L type Calcium chan...

**[Chapter 14 -- Cardiovascular Physiology \~ Start of Exam 3]** 1. [Describe the membrane proteins and ion movement involved in myocardial excitation-contraction (EC) coupling and relaxation]. **CONTRACTION**: AP starts in pacemaker cell & AP enters from adjacent cell L type Calcium channel on cell membrane opens Ca enters from the ECF RYR calcium channel on SR releases more calcium calcium induced calcium release Calcium spark & Ca summed signal Ca binds to troponin, cross bridge cycle like SKM **RELAXATION**: after contraction, Ca is pumped back via ATPase into SR for storage Ca is exchanged with sodium by the NCX antiporter (Ca is actively transported out of contractile cell) / sodium that just entered via the antiporter is quickly transported back out of cell via the sodium potassium ATPase pump (2 K+ in... 3 Na+ out) A diagram of a cell cycle Description automatically generated **Compare this with SKM & Smooth muscle** - **Smooth -- Ca2+ induced Ca2+ released = similarity** - **SKM -- binds to troponin = similarity** 2. [Compare and contrast action potentials of myocardial autorhythmic and contractile cells. ] **REVIEW GRAPH IN NOTES** **\*\*\*I GOT MUNCHED ON THIS ON THE TEST** Autorhythmic vs Contractile cells - Autorhythmic = pacemakers - Small and few in number - Unstable membrane potential "pacemaker potential" from iF channels - Enables continuous depolarization to set heartbeat without external output - Contractile cells - Striated, organized into sarcomeres - Stable membrane potential - Depolarization initiated via gap junction from adjacent cell - Extended plateu from Ca entry LONGER CONTRACTION - Longer refractory period PREVENTS TETANUS  A diagram of a graph Description automatically generated with medium confidence  3. Explain the relationship of heart rate, cardiac output, and stroke volume. **CO = HR x Stroke volume** - Average = 5L/min - [Stroke volume] = amount of blood volume pumped per 1 ventricular contraction - Stroke volume = EDV - ESV - [Ejection fraction] = percent of end diastolic volume (EDV) ejected per 1 ventricular contraction... is a measure to evaluate ventricular fraction - Ejection fraction = stroke volume/EDV 4. Explain the role of the autonomic divisions in control of heart rate at the cellular and molecular level. Act on ion channels and change permeability! **Sympathetic neurons:** - **Uses norepinephrine and epinephrine acting on B1 receptors make membrane more permeable to sodium and calcium faster depolarization increase HR** - **Epi & Norepi increase contraction force & shorten duration of contraction (FASTER)** **Parasympathetic neurons:** - **Acetylcholine activates muscarinic receptors to make membrane more permeable to K+ leaving the cell hyperpolarize lower HR** **Tonic control \~ normally dominated by PNS activity** A screenshot of a diagram Description automatically generated  5. Explain how the following factors influence stroke volume: venous return, length- tension relationships, preload, afterload, contractility, skeletal muscle pump, respiratory pump, inotropic agents. **Afterload seemed to be an area that should be reviewed.** EDV affects stretch of heart affects stroke volume (SV) - Venous return determines the EDV and preload (degree of stretch) - Venous return is determined by: skeletal muscle pump, respiratory pump, sympathetic innervation of veins (dilation) - \*More venous return more EDV greater stroke volume Longer length = greater tension = greater force of contraction Catecholamines like norepinephrine can increase contractility (force of contraction) without changing stretch Inotropic agent = any chemical affecting contractility - Positive inotropes = increase contractility - Norepinephrine and epinephrine - Negative inotropes = decrease contractility Afterload = load placed on ventricle as it contracts... combined load of EDV + arterial resistance during ventricular contraction - EDV and arterial blood pressure (which must be overcome/surpassed) determines Afterload - \*\*\*afterload is unique because increased afterload DECREASES stroke volume A diagram of a process Description automatically generated